Current Concepts in the Prevention of Perioperative Myocardial Injury.

Christian Bohringer, Duc Le, Hong Liu
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Abstract

Perioperative myocardial injury is frequently caused by tachycardia from excessive sympathetic nervous system activity resulting from the surgical stimulation (type 2) rather than by rupture of atherosclerotic plaques with superimposed thrombosis (type 1). The elevated sympathetic nervous system activity results in tachycardia that induces demand ischemia within the myocardium and damages the heart muscle. A rise in troponin has been shown to be a reliable predictor of adverse cardiovascular events when measured in a population at risk. This holds true even when the troponin rise is isolated and other markers for myocardial damage like prolonged ischemic type chest pain, new electrocardiogram changes or evidence of new myocardial damage on echocardiography and other cardiac imaging studies are absent. Treatments that prevent tachycardia by successfully controlling elevated sympathetic tone, like dexmedetomidine and thoracic epidural blockade with local anesthetic reduce troponin release and have been shown to prevent myocardial damage. Intravenous lidocaine and magnesium can also prevent tachycardia. Beta blockers reduce myocardial injury, but are associated with an increase in hypotension and ischemic stroke. Any method of attenuating sympathetic nervous system activity, may however, require treatment with intravenous fluids and vasopressors to prevent hypotension. Rupture of atherosclerotic plaques with superimposed coronary thrombosis is a far less common cause of myocardial infarction in the perioperative period than elevated sympathetic tone. This explains why prophylactic statins in previously statin-naïve patients do not reduce major adverse cardiovascular event rates. Antiplatelet agents are also ineffective in reducing adverse cardiovascular events in the perioperative period. Clinicians, therefore, need to focus their attention on heart rate control and the attenuation of the stress response to surgery, rather than on atherosclerotic plaque stability and antiplatelet drugs in order to successfully prevent perioperative myocardial injury.

Abstract Image

预防围手术期心肌损伤的最新概念
围手术期心肌损伤通常是由手术刺激引起的交感神经系统过度活动引起的心动过速引起的(2型),而不是由动脉粥样硬化斑块破裂和叠加血栓形成引起的(1型)。交感神经系统活动的升高导致心动过速,心动过速会在心肌内引发需求性缺血并损害心肌。肌钙蛋白的升高已被证明是风险人群中心血管不良事件的可靠预测指标。即使肌钙蛋白升高是孤立的,并且心肌损伤的其他标志物,如长期缺血性胸痛、新的心电图变化或超声心动图和其他心脏成像研究中没有新的心肌损伤的证据,这一点也是正确的。通过成功控制交感神经张力升高来预防心动过速的治疗方法,如右美托咪定和局部麻醉剂胸段硬膜外阻滞,可以减少肌钙蛋白的释放,并已被证明可以预防心肌损伤。静脉注射利多卡因和镁也可以预防心动过速。β受体阻滞剂可减少心肌损伤,但与低血压和缺血性中风的增加有关。然而,任何减弱交感神经系统活动的方法都可能需要静脉输液和血管升压药来预防低血压。动脉粥样硬化斑块破裂并叠加冠状动脉血栓形成是围手术期心肌梗死的常见原因,远低于交感神经张力升高。这就解释了为什么在以前服用他汀类药物的幼稚患者中使用预防性他汀类药物并不能降低主要心血管不良事件的发生率。抗血小板药物在减少围手术期心血管不良事件方面也无效。因此,临床医生需要将注意力集中在心率控制和减轻手术应激反应上,而不是动脉粥样硬化斑块的稳定性和抗血小板药物上,以成功预防围手术期心肌损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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